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Molly Hinshaw, MD

Arch Dermatol. 2006;142:512-513.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

Use of Human Tissue to Assess the Oncogenic Activity of Melanoma-Associated Mutations
Chudnovsky Y, Adams AE, Robbins PB, Lin Q, Khavari PA.
Nat Gen. 2005;37:745-749.

Multiple genetic alterations occur in melanoma, a lethal skin malignancy of increasing incidence. These include mutations that activate Ras and two of its effector cascades, Raf and phosphoinositide 3-kinase (PI3K). Induction of Ras and Raf can be caused by active N-Ras and B-Raf mutants as well as by gene amplification. Activation of PI3K pathway components occurs by PTEN loss and by AKT3 amplification. Melanomas also commonly show impairment of the p16^INK4A-CDK4-Rb and ARF-HDM2-p53 tumor suppressor pathways. CDKN2A mutations can produce p16 ^INK4A and ARF protein loss. Rb bypass can also occur through activation CDK4 mutations as well as by CDK4 amplification. In addition to ARF deletion, p53 pathway disruption can result from dominant negative TP53 mutations. TERT amplification also occurs in . . . [Full Text of this Article]

COMMENT

AUTHOR INFORMATION

Department of Dermatology, Anschutz Cancer Pavilion, Aurora, Colo